This is consistent with a previous conclusion that the genes with functional variants associated with proinflammatory Th17 pathway-associated molecules and with immune diseases such as Crohn's disease do not alter T1D risk (e.g. CCR6 and IL23R) 1, even though the role of proinflammatory cytokines, IL-1β, TNF-α and IL-17, in pancreatic β cell killing is established. This evidence concerns the gene IL23R and type 1 diabetes mellitus.